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Pharm Tox > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Only ________ Black widows are Dangerous.

A

Female

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2
Q

Primary toxin released from Black widows is?

A

Alpha-Latrotoxin

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3
Q

What is the result of Alpha-Latrotoxin released by black widow’s?

A

Releases neurotransmitters
- ACh
- Norepinephrine
- Dopamine
- Glutamate
- Enkephalins

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4
Q

Black widow bite produces what type of lesion?

A

Target Lesion

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5
Q

Black widow venom is a ________ toxin.

A

Nerve

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6
Q

Clinical Signs of Black Widow bite: (5)

A

1) Muscle Spasm
2) Painful Rigidity of Abdomen
3) Chest Tightness
4) Increased body temp
5) Localized Swelling

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7
Q

First aid for black widow bite:

A

Clean the wound & apply ice

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8
Q

Most effective treatment of black widow bite?

A

Anti venom “Lyovac” (Latrodectus

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9
Q

What is the goal of Black Widow Bite treatment?

A

Stop muscle spasms

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10
Q

How to identify the Brown recluse spider:

A
  • Has 3 pairs of eyes
  • “Fiddle back spider” / “Violin spider”
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11
Q

Are Males or Females toxic (Brown Reclluse Spider)?

A

Both, but female has more venom

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12
Q

What enzyme is the toxin in Brown recluse spiders?

A

Spingomyelinase D Enzyme

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13
Q

What does Spingomyelinase D Enzyme cause in the body from the brown recluse spider?

A

1) Binds to cell membrane -> Chemotaxis
2) Attracts PMN’s -> Tissue Destruction

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14
Q

What is the spreading factor of a brown recluse spider bite?

A

Hyaluronidase

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15
Q

Clinical signs of a Brown Recluse spider bite:

A
  • Bull’s Eye Lesion
  • Red area that turns into a sore
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16
Q

Medical treatment used for a brown recluse spider bite:

A

Dapsone (a leukocyte inhibitor)

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17
Q

Aggression in Bees is triggered by _____ and they attack ______ colors.

A

CO2; dark

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18
Q

Main peptides & proteins in bee venom:

A

1) Peptide 401
2) Apamin
3) Melittin

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19
Q

Primary Enzymes in bee venom:

A

Phospholipase A2 & Hyaluronidase

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20
Q

How many bee stings does it take to illicit allergic death?

A

One

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21
Q

Clinical signs of a bee sting: (6)

A

1) Renal failure
2) Rhabdomyolysis
3) Optic neuritis
4) Atrial flutter
5) Hepatic dysfunction
6) Respiratory. Distress

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22
Q

How do you remove a bee’s stinger from the skin?

A

Scrape it off. Squeezing can release more venom from the sac.

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23
Q

Yellow Jackets do not have __________ _____________ so they can sting you ____________ ________.

A

Barbed Stingers; Multiple times

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24
Q

Major Venom components of a yellow jacket (wasp): (5)

A

1) Phospholipase
2) Hyaluronidase
3) Cholinesterase
4) Mastoparans
5) Amines

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25
Q

Local clinical signs of a wasp sting: (4)

A

1) Redness
2) Edema
3) Erythema
4) Pruritis

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26
Q

Systemic clinical signs of wasp sting: (8)

A

1) Anaphylaxis
2) Hemolysis
3) Renal failure
4) encephalopathy
5) hepatotoxicity
6) optic neuritis
7) Hyperkalemia
8) Rhabdomyolysis

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27
Q

Math the disease to its carrier:

1) RMSF
2) Lyme Disease
3) Bubonic Plague

  • Ixodes Tick
  • Dermacentor Tick
  • Fleas
A

1) RMSF. Dermacentor Tick
2) Lyme Disease. Ixodes Tick
3) Bubonic Plague. Fleas

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28
Q

The Black Legged tick (Deer tick) transmits:

A

Borrelia Burgdorferi & Lyme Disease

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29
Q

Brown dog tick transmits:

A

Rhipicephalus Sanguineus

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30
Q

What has the most active venoms of the “Hymenoptera”?

A

Ants

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31
Q

How do ants deliver their venom?

A

They bite, then move the stinger down

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32
Q

Field ant venom is high in ___________.

A

Formic Acid

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33
Q

Fire ant venom is a necrotizing ___________, and does what?

A

Alkaloid; that inhibits Sodium, Potassium & ATPase pumps in postsynaptic neuromuscular junctions.

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34
Q

What species has become the most lethal known venom of any animal in the New World?

A

Harvester Ant Venom

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35
Q

Systemic clinical signs of fire ant venom: (3)

A

1) Seizures
2) Intravascular Coagulopathy
3) Rhabdomyolysis

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36
Q

General care for Ant bites:

A
  • Topical corticosteroids
  • Antihistamines
  • Camphor
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37
Q

What is used to denature Formic Acid from ant bites?

A

NaOCl

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38
Q

MC location of Poisonings

A

92.7% at a residence

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39
Q

What percent of poisonings occur in children younger than __________-.

A

50.9% / Six years

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40
Q

56% of poisoning fatalities occurred in what age group?

A

20-49 year olds

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41
Q

MC route of exposure for poisonings:

A

Oral Ingestion 70%

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42
Q

What is the primary agent responsible for fatalities?

A

Analgesics

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43
Q

MC reason for exposure to poisonings & %

A

Unintentional (83.8%)

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44
Q

Most poisonings occur at what time?

A

At home just before meal time

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45
Q

More people die in the US from ________ than from ____________.

A

Suicides; Homicides

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46
Q

Standard treatment for poisonings: (4 steps)

A

1) ABC’s
2) Support the patient
3) Protect the Airway
4) Give Activated Charcoal

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47
Q

Top 3 substances involved in human exposures & their percentages:

A

1) Analgesics - 11.7%
2) Cosmetics & personal care products - 9.2%
3) Cleaning substances - 9%

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48
Q

MC substance involved in PEDIATRIC poison exposures:

A

Cosmetics & Personal care products (13.4%)

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49
Q

Definition of Toxicology

A

The study of poisons

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50
Q

Definition of Hazard:

A

Likelihood an event will occur based on how the product is packaged, formulated or its accessibility

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51
Q

Definition of Risk:

A

Probability that an event will occur based on patient vulnerability

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52
Q

Definition of Toxic Substance

A

Poisons

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53
Q

Definition of Poison:

A

Any chemical substance which can cause harm

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54
Q

Definition of Antidote:

A

Remedy for counteracting a poison

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55
Q

What are the 3 types of Antidotes & what do they do?

A

1) Chemical: react to form harmless compound
2) Mechanical: prevents absorption
3) Physiologic: counteracts the effects

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56
Q

Emergency actions for non-specific poisons include: (4)

A

1) Symptomatic? -> Call 911
2) Maintain airway
3) Vital signs
4) Supportive care

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57
Q

MOI of Carbon Monoxide poisoning:

A

1) CO binds to Hb creating Carboxyhemoglobin
2) Impairs O2 delivery to tissues
3) Especially affects Heart & Brain
4) Causes Cellular Hypoxia

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58
Q

Signs & Symptoms of Carbon Monoxide Poisoning: (3)

A

1) Depend on % of CO-Hb levels in blood
2) Cherry red blood is Pathognomic
3) Pt. Is NOT Cyanotic

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59
Q

Mild Clinical grading of Carbon Monoxide Poisoning Symptoms: (4)

A

1) Headache
2) nausea/Vomiting
3) Dizziness
4) Flu-Like symptoms

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60
Q

Moderate Clinical grading of Carbon Monoxide Poisoning Symptoms: (6)

A

1) Confusion/Slow thinking
2) SOB
3) Blurred vision
4) Tachycardia & Tachypnea
5) Ataxia
6) Weakness

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61
Q

Severe Clinical grading of Carbon Monoxide Poisoning Symptoms: (7)

A

1) Palpitations/Chest Pain
2) Drowsiness
3) Disorientation
4) Hypotension
5) Syncope
6) MI
7) Pulmonary Edema

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62
Q

Antidote for Carbon Monoxide Toxicity:

A

100% Oxygen

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63
Q

MC route of exposure for Heavy Metal toxicity:

A

Oral (secondary is inhalation of fumes)

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64
Q

Heavy metal toxicity is expressed _____________ because of their ability to bind one or more __________ of __________ ____________ __________ which then _____________ the enzyme system.

A

Biologically; Ligands; Biologic Enzyme Systems; Inactivates

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65
Q

Antidote for heavy metal poisonings:

A

Chelating agents

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66
Q

Chelating Agents ___________ inactivate heavy metal poisons.

A

Chemically

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67
Q

Chelates are ____________ and are excreted by the __________.

A

Water-soluble; kidneys

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68
Q

Example of Chelating agent & what it is used for:

A

Calcium Disodium (EDTA); lead toxicity

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69
Q

Calcium Disodium (EDTA) as a chelating agent can cause:

A
  • Renal issues
  • Fever
  • Dermatitis
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70
Q

What is the most significant of the heavy metal poisonings?

A

Lead

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71
Q

What is the most critical aspect of diagnosing lead poisoning?

A

Pt. History

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72
Q

What is the most important chronic environmental illness affecting modern children?

A

Lead poisoning

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73
Q

What organ is the most concerned in lead poisoning?

A

the Developing brain

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74
Q

Lead Poisoning in children produces long-term problems with: (3)

A

1) Learning
2) Intelligence
3) Earning Power

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75
Q

Adults with lead poisoning have problems with: (3)

A

1) Depression
2) Aggressive Behavior
3) Antisocial Behavior

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76
Q

Males with lead poisoning have…

A

Lower sperm counts

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77
Q

Females with lead poisoning have…

A

Increased incidence of miscarriage and smaller babies

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78
Q

Clinical Features of Plumbism (Acute Lead Intoxication) (7)

A

1) Colic
2) Metallic taste in mouth
3) Vomiting, diarrhea or constipation
4) Increased thirst
5) Hemolysis
6) Oliguria
7) Paresis and Paresthesia

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79
Q

Other health effects of Lead poisoning: (6)

A

1) Slow growth/development
2) anorexia
3) renal damage
4) drowsiness
5) paralysis
6) premature birth

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80
Q

Signs & Symptoms of chronic lead poisoning: (5)

A

1) Burtonian Line
2) basophilic stippling
3) Anemia
4) Colic, diarrhea, vomiting
5) muscle weakness

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81
Q

Chronic lead toxicity can cause increased density at the ____________ of ___________ bones.

A

Metaphyses; Tubular (growing)

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82
Q

Lead lines are MCly seen in what 2 bones?

A

Proximal Fibula & Distal Ulna

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83
Q

What abnormality in lead poisoning is seen in the Distal femur?

A

Erlenmeyer Flask Appearance

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84
Q

Lead Palsy results in: (2)

A

1) Wrist Drop (radial)
2) Foot drop (common fibular)

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85
Q

Treatment for acute lead intoxication: (4)

A

1) Induce vomiting
2) Give cathartics
3) Give proteins (milk, egg. White)
4) Chelating Agents

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86
Q

Treatment for Chronic Lead toxicity:

A

Chelating agents

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87
Q

Iron toxicity is seen mostly in __________.

A

Children

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88
Q

MOI of Iron toxicity: (6)

A

1) occurs. When iron levels > binding capacity of transferrin
2) damages tissue by Direct Corrosive Effects
3) Injures Blood vessels
4) Hepatocellular Death via Hemochromatosis
5) Metabolic Acidosis
6) Coagulation issues

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89
Q

Iron is irritating to the _______ _________.

A

gastric mucosa

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90
Q

Once absorbed, iron is taken up by what cells?

A

Liver cells

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91
Q

What 2 things does mitochondrial poison do?

A

1) Disrupts electron transport chain
2) Inhibits oxidative Phosphorylation

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92
Q

Stage 1 of Iron toxicity signs: (3)

A
  • Acute GI corrosive effects
  • Hematochezia
  • Melena
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93
Q

Stage 2 of Iron Toxicity signs: (1)

A

Sometimes called Latent/Quiescent period
1) Resolution of GI symptoms

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94
Q

Stage 3 of Iron Toxicity Signs: (2)

A

1) Recurrance of GI hemorrhage
2) Death is common in this stage

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95
Q

Stage 4 of Iron toxicity Signs: (2)

A

1) Gastirc Outlet Obstruction
2) Pyloric Stenosis

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96
Q

What time does each stage of Iron Toxicity occur (post-ingestion)?

A

1: 30 min-6 hours
2: 6-24hrs
3: 12-48hrs
4: 4-6 weeks

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97
Q

Chronic Iron Toxicity is associated with: (5)

A

1) Pigmented Hepatic Cirrhosis
2) Diabetes Mellitus
3) Hyperpigmentation of the Skin
4) Hemosiderosis
5) Hemochromatosis

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98
Q

Treatment for Chronic Iron Toxicity: (4)

A

1) Induce vomiting
2) Activated Charcoal (NO HELP)
3) Transport
4) Chelators like Deferoxamine

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99
Q

Mercury toxicity can be caused by:

A

Dental Amalgam Fillings

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100
Q

What type of mercury passes through the placenta and maternal exposure can lead to spontaneous abortion or retardation?

A

Methylmercury

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101
Q

What vaporizes easily at room temperature?

A

Elemental mercury (Quicksilver)

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102
Q

What type of mercury is found in thermometers, amalgams & manometers?

A

Elemental mercury (Quicksilver)

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103
Q

Clinical Signs of elemental (quicksilver) toxicity: (5)

A

1) Pulmonary symptoms
2) Fever/chills
3) Dyspnea
4) lethargy/confusion
5) can be misdiagnosed as parkinson’s/alzheimers

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104
Q

Treatment for elemental (quicksilver) toxicity:

A

ABC’s, O2 & Chelation

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105
Q

2 routes of exposure for Inorganic Mercury (mercurial salts) toxicity:

A

1) Oral
2) GIT

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106
Q

Source of Inorganic Mercury (mercurial salts) Toxicity: (2)

A

1) Disc batteries
2) Mercurous Chloride

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107
Q

Signs & Symptoms for Inorganic Mercury (mercurial salts) Toxicity:

A

1) Ashen gray mucous membranes
2) Severe abdominal pain
3) Hematemesis
4) Loose Teeth
5) Renal tubular necrosis

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108
Q

Treatment for Inorganic Mercury (mercurial salts) Toxicity:

A

ABC’s & Chelation therapy

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109
Q

Organic mercury (methyl mercury) results from ingestion of:

A

Contaminated food such as
- Shell fish
- Tuna
- Shark

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110
Q

How long does Organic mercury (methyl mercury) remain in your body after ingestion?

A

4-6 weeks

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111
Q

Where is Organic mercury (methyl mercury) eliminated in the body?

A

Bile

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112
Q

What must occur in the body before symptoms arise with Organic mercury (methyl mercury) toxicity?

A

Target enzymes and depletion of these enzymes (days to weeks before symptoms)

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113
Q

Clinical presentation of Organic mercury (methyl mercury) toxicity: (6)

A

1) Visual disturbances
2) Ataxia
3) Hearing loss
4) Mental deterioration
5) Muscle Tremors
6) Paralysis

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114
Q

What is Thimerosal?

A

Organic Mercurial Compound with 49.6% Ethyl Mercury

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115
Q

What was formerly used as a preservative in pediatric vaccines to prevent bacterial contamintion?

A

Thimerosal

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116
Q

Thimerosal is ________ soluble and eliminated through the _________.

A

Water; Urine

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117
Q

How fast is Ethyl Mercury eliminated from the body?

A

3-6x faster than the environmental form “methyl mercury”

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118
Q

What is the 1/2 life of ethyl mercury compared to Methyl mercury in infants who have been given vaccines?

A

Ethyl: 6-8 days
Methyl: 45 days

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119
Q

What type of vaccines still have mercury in them today?

A

Multi-dose vial flu shots (Fluzone, Sanofi Pasteur & Fluvirin)

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120
Q

Thimerosal (Ethyl Mercury) Diagnosis is based on: (2)

A

1) Pt. History & clinical signs
2) Urinary Mercury levels greater than 20-25 ug/L

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121
Q

Treatment for Acute Thimerosal (Ethyl mercury) toxicity:

A

Same as any poison

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122
Q

Treatment for Chronic Thimerosal (Ethyl mercury) toxicity:

A

Chelation therapy (BAL)

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123
Q

What heavy metal is a natural element found in soil & minerals?

A

Arsenic

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124
Q

What heavy metal commonly contaminates well water?

A

Arsenic

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125
Q

What heavy metal is tasteless and resembles sugar?

A

Arsenic

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126
Q

Arsenic exposure is typically (3 things):

A

1) Suicidal
2) Homicidal
3) Occupational

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127
Q

You may be exposed to Arsenic by slowly…

A

1) taking in small amounts in food, water or air
2) breathing in sawdust or burning arsenic-treated wood

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128
Q

Food sources of Arsenic: (4)

A

1) Rice Products (Baby foods)
2) Ground water
3) Apple & Grape juice
4) Red wine

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129
Q

MOI of Arsenic:

A

Inhibition of Sulfhydryl enzymes replaced by Phosphate molecules in high energy compounds

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130
Q

What type of arsenic is a carcinogen & what type of cancer results?

A

Trivalent Arsenic; lung & skin cancer

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131
Q

What is the most toxic form of Arsenic?

A

Trivalent Arsenic

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132
Q

Where can Trivalent Arsenic be recovered from on the body?

A

Skin, Hair & Nails

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133
Q

Clinical presentation of Acute Arsenic Poisoning: (5)

A

1) Profuse diarrhea (rice water stool)
2) Garlic odor to breath
3) Dark urine
4) Vertigo, shock & death
5) Hemolysis

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134
Q

What types of cancer are increased with Arsenic poisoning?

A

Lung, Bladder/Kidney & Liver

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135
Q

Clinical Signs of Chronic Arsenic Toxicity: (5)

A

1) Palmar and Plantar hyperkeratosis (skin bumps)
2) Anemia (milk & roses complexion)
3) Gangrene Feet ( Blackfoot disease)
4) Anorexia/GI Symptoms
5) Encephalopathy

136
Q

Diagnosis of Arsenic toxicity:

A

Urine sample = most reliable
> 200 ug/L is abnormal

137
Q

Treatment for arsenic toxicity: (2)

A

1) Support airway, breathing & circulation
2) Chelation therapy

138
Q

What is Chlorella?

A

From Algae: natural immune stimulant and has a high affinity for heavy metals

139
Q

What foods aid in the removal of heavy metals?

A

Garlic, Onions & cilantro

140
Q

What are the 3 MC alcohol poisonings:

A

1) Ethanol
2) Isopropanol
3) Methanol

141
Q

Acute intoxication with any alcohol can result in: (4)

A

1) Coma
2) Respiratory depression
3) CV collapse due to CNS depression
4) aspiration of vomitus

142
Q

Ethanol is what type of alcohol?

A

Aliphatic

143
Q

Ethanol is found in: (4)

A

1) aftershaves, cologne, perfumes
2) mouthwash
3) OTC meds
4) alcoholic beverages

144
Q

Ethanol is a direct ______ ___________ which causes decreased _________ & ___________ levels.

A

CNS depressant; Motor & Consciousness

145
Q

Ethyl Alcohol is also known as:

A

Grain alcohol

146
Q

Ethyl alcohol is derived from:

A

Fermentation of sugars in fruits, cereals and vegetables

147
Q

What is the “proof” of Ethyl alcohol?

A

100 proof = 50% alcohol

148
Q

When the stomach is empty, peak levels of Ethanol absorption occurs at?

A

30-90 minutes (total absorption can take 6 hours)

149
Q

Metabolism of ethanol is carried out by the?

A

Liver

150
Q

What liver enzymes metabolize ethanol?

A

1) Alcohol dehydrogenase
2) aldehyde dehydrogenase
3) MEOS (5%, but increases to 25% in alcoholics)

151
Q

Nonhabituated patients metabolize how much ethanol per hour?

A

13-25 mg/dL/h

152
Q

What is the primary source of ingested Ethanol?

A

Alcoholic beverages

153
Q

Associated problems with ethanol ingestion include: (4)

A

1) Hypoglycemia
2) head trauma
3) carbon dioxide narcosis
4) hypoxia

154
Q

How do. You calculate BAC?

A

[0.8 ml 90% ethanol / kg body weight = BAC]

220 lb Male -> 100 kg Male -> 80ml or a little less than 3 ounces of 90% or 180 proof or 6 beers = BAC of 0.08%

155
Q

Long term effects of ethanol toxicity: (5)

A

1) Hepatic Cirrhosis
2) Esophageal cancer
3) pancreatic cancer
4) Wernicke’s syndrome
5) B vitamin deficiencies/malnutrition

156
Q

Treatment for ethanol toxicity:

A

1) keep pt. From injury inf themselves
2) protect airway
3) Disulfuram blocks acetaldehyde dehydrogenase causing build up of aldehyde

157
Q

Methyl alcohol is AKA:

A

Wood alcohol

158
Q

Sources of Methanol:

A
  • Cleaning fluids, solvents, paints
  • Windsheild washer fluid
  • Moonshine
159
Q

What is the fatal dose of Methanol?

A

30-240ml

160
Q

MOI of the metabolism of methanol:

A

Methanol -> Formaldehyde -> Formic Acid -> CO2 +H20

161
Q

What alcohol has a profound metabolic acidosis and blindness associated with it?

A

Methanol

162
Q

What does Methanol do to the eye? (7)

A

Formic acid inhibits cytochrome oxidase in the fundus.
- disrupts axoplasmic flow
- swelling of axons
- optic disc edema
- blurred vision
- yellow spots
- snowstorm vision
- photophobia

163
Q

What type of respiration is seen in Methanol toxicity?

A

Kussmaul’s respiration (tachypnea & dyspnea)

164
Q

Treatment of methanol ingestion: (4)

A

1) ETHANOL
2) Fomepizole (anti oil)
3) airway/breathing support
4) folic acid

165
Q

Isopropyl is AKA:

A

Rubbing alcohol

166
Q

What is the 2nd MCly consumes alcohol?

A

Isopropyl

167
Q

What is the lethal dose of isopropyl?

A

240ml

168
Q

Clinical presentation of Isopropyl toxicity:

A

1) Headache, dizziness
2) ataxia, nystagmus
3) abdominal pain, hematemesis
4) might have fruity breath

169
Q

Isopropanol is metabolized to acetone by _____

A

ADH

170
Q

Treatment for Isopropyl toxicity: (3)

A

1) gastric lavage
2) activated charcoal
3) airway support

171
Q

What alcohol is a clear, colorless, odorless, viscous fluid with a bittersweet aftertaste?

A

Ethylene glycol

172
Q

What is the source of ethylene gylycol?

A

Antifreeze

173
Q

Is ethylene glycol toxic?

A

Not by itself, but its metabolites are highly toxic

174
Q

Ethylene glycol combines with calcium to form:

A

Calcium oxalate crystals

175
Q

Lethal dose of ethylene glycol:

A

100ml

176
Q

What happens in the body with ethylene glycol toxicity? (3)

A

Tissue destruction
- precipitation of calcium oxalate in tissues
- especially renal cortex
- severe metabolic acidosis

177
Q

Phase 1 Clinical presentation of Ethylene Glycol toxicity:

A
  • Inebriated
  • nauseated
  • vomiting
  • ataxia
  • no alcohol smell on breath
178
Q

Phase 2 Clinical presentation of Ethylene Glycol toxicity:

A
  • tachycardia/elevated BP
  • pulmonary edema/tachypnea
  • cardiac failure
  • calcium oxalate crystals deposited in vascular tree, lungs & heart
179
Q

Phase 3 Clinical presentation of Ethylene Glycol toxicity:

A
  • flank pain
  • costovertebral angle tenderness
  • Oliguric acute renal failure
180
Q

Time frame for Phases 1-3 of Ethylene glycol toxicity (after ingestion)

A

1: 30-12hrs
2: 12-24hrs
3: 24-72hrs

181
Q

Diagnoses of Ethylene glycol toxicity: (4)

A

1) drunk with NO alcohol smell on breath
2) Calcium oxalate crystals in urine
3) renal failure
4) Kussmaul’s Respiration

182
Q

What enzyme converts Ethylene Glycol into Oxalic Acid?

A

Alcohol Dehydrogenase

183
Q

Ethylene Glycol toxicity treatment: (4)

A

1) Treat acidosis
2) Ethyl alcohol
3) Thiamine
4) Water-soluble vitamin B complex

184
Q

Corrosive vs. Caustic (denotes a ________ substance)

A

Corrosive: ACIDIC
Caustic: ALKALINE

185
Q

MOI of Acids:

A

[Denature proteins]
- Coagulative necrosis
- tough leathery eschar or coagulum

186
Q

What is the MCly involved organ in acid toxicity?

A

Stomach

187
Q

If a pt. Has ingested an acid…

A

ANY ingestion constitutes a medical emergency

188
Q

If acid has come in contact with the skin or eyes…

A

Flush with water. Remove jewelry & contacts & wash with soap

189
Q

Do you give water to someone who has swallowed an acid?

A

NO it will have an exothermic reaction. Do not induce vomiting & maintain airway

190
Q

Clinical concerns with acid ingestion:

A

1) perforation after 3rd or 4th day as eschar sloughs
2) gastric obstruction may develop over 2-4 week period
3) upper GIT hemorrhage

191
Q

What is more common acid or alkali toxicity?

A

Alkali

192
Q

MC alkali agents that cause toxicity:

A

Ammonia & Sodium Hydroxide

193
Q

Most cases of alkali toxicity are what age group?

A

Children under 5

194
Q

MOI of alkali toxicity:

A

1) Liquefactive necrosis -> tissue injury
2) cell death from emulsification of membranes

195
Q

What tissue are most severely injured with alkali toxicity?

A

Squamous epithelial cells of oropharynx & esophagus

196
Q

Alkali burns to the skin appear:

A

Yellow, soapy & soft

197
Q

Clinical concerns for alkali toxicity: (5)

A

1) Edema
2) Erythema
3) Ulceration
4) Necrosis
5) Perforation

198
Q

What can you give orally to a pt. With alkali toxicity?

A

Milk, water or egg whites

199
Q

Mixing bleach with acid or alkali cleaning or ducts releases:

A

Chlorine gas

200
Q

Petroleum Distillates are produced from

A

Fractional distillation of crude petroleum

201
Q

Major threat of Hydrocarbon toxicity is:

A

Aspiration Pneumonitis (vomiting increases this risk)

202
Q

When aspirated (in hydrocarbon toxicity), petroleum distillates…

A

Inhibit surfactant causing alveolar collapse -> hypoxemia

203
Q

Signs & Symptoms of pulmonary involvement in hydrocarbon toxicity: (4)

A

1) coughing, gasping, choking
2) gasoline breath
3) Rales & wheezes on auscultation
4) Hemoptysis & pulmonary edema

204
Q

Signs & Symptoms of CNS involvement in hydrocarbon toxicity: (3)

A

1) Dyspnea
2) syncope
3) cuddles cardiac death

205
Q

What should you NOT do with hydrocarbon toxicity?

A

DO NOT induce vomiting as it increases the risk of aspiration pneumonitis

206
Q

What you SHOULD do in hydrocarbon toxicity:

A

Maintain airway & support respiration

207
Q

Sources of alkali toxic substances: (6)

A

1) Drain cleaners
2) oven cleaners
3) swimming pool
4) dishwasher detergent
5) disc batteries
6) soaps & bleach

208
Q

what is the most extensively used illicit drug?

A

Weed

209
Q

What is the active ingredient in weed?

A

Tetrahydrocannabinol (THC)

210
Q

Where in the plant is the highest concentration of THC found?

A

Leaves and flowering tops

211
Q

An average joint contains how much THC?

A

15-30mg

212
Q

Weed has how many active chemicals?

A

Over 400

213
Q

What drug is used to treat nausea and vomiting associated with chemo therapy?

A

Dronabinol (Marino)

214
Q

Where is weed excreted in the body?

A

15-50% in the urine & feces

215
Q

Weed detection is done by measuring…

A

Urine levels of THC carboxylic acid

216
Q

What effect does weed have in the body?

A
  • Binds to cannabinoid receptors CB1 & CB2
  • Potentiates receptors causing brain to forget experiences
217
Q

Cannabinoid Receptors are mostly located where? Where are ther very few?

A

Many: (Cognition & movement affected)
Basal Ganglia, Hippocampus, Cerebellum

Few: (Heart & lungs)
Lower brain stem

218
Q

Acute effects of Weed usage: (7)

A

1) Sinus tachycardia
2) Orthostatic hypotension
3) Elevated BP
4) Increased Myocardial Oxygen demand
5) Short-term memory impairment
6) Xerostomia
7) Rhinitis

219
Q

Treatment for acute intoxication of weed:

A

Place pt. In a dark room & treat symptoms accordingly

220
Q

Weed compromises the ability to ______ and ____________ _____________ which can last for ________ or ___________.

A

Learn; Remember Information
Days; Weeks

221
Q

In a 2019 study of 129 college students, what skills were impaired by those who smoked weed?

A

Attention, Memory & Learning

222
Q

Therapeutic effects of smoking weed: (6)

A

1) Antitumor effect
2) Antiemetic
3) Appetite stimulant
4) Analgesic
5) Anxiolytic
6) Sleep Wake

223
Q

Weed usage can lead to what conditions? (4)

A

1) Chronic bronchitis episodes
2) Increased risk of MVA
3) Decreased birth weight
4) Increased schizophrenia risk

224
Q

MOI of Cocaine:

A
  • Causes central and peripheral blockage of the re-uptake of catecholamines
  • Blocks sodium channels (local anesthetic)
  • Buildup of Dopamine in the SYNAPSE
225
Q

Cocaine is classified as a

A

Stimulant-benzoylmethylecgonine

226
Q

What drug was formerly used in rhinoplasty?

A

Cocaine

227
Q

What is the serum half life of cocaine?

A

30-80 minutes

228
Q

What plant are opiates derived from?

A

Poppy plant

229
Q

Examples of Opiates (3)

A

Oxycodone
Hydrocodone
Fentanyl

230
Q

What drug has a high risk of Respiratory depression?

A

Opiates

231
Q

What are the classic signs of an opioid overdose?

A

The classic triad:
1) Pinpoint Pupils
2) Unconsciousness
3) Respiratory Depression

232
Q

CNS effects of Opiates: (3)

A

1) Respiratory depression
2) sedation/ euphoria
3) nausea & vomiting

233
Q

CVS effects of Opiates: (2)

A

1) Peripheral dilation
2) Hypotension/Brady cardia

234
Q

GI Effects of Opiates: (3)

A

1) Decreased motility
2) Contipation
3) Miosis

235
Q

What drug is used as treatment for Opiate overdose? What is it?

A

Naloxone (opioid receptor antagonist)

236
Q

What is the most abused & most rapidly acting Opiate?

A

Heroin

237
Q

Heroin is extracted from what plant?

A

Seed pod of poppy plants

238
Q

Mexican Heroid is also known as

A

Black tar

239
Q

Buprenorphine is sold under the name ________, and used to treat ___________ ____________.

A

Subutex; Opioid Addiction
Methadone (Dolophine) is also used

240
Q

Most sedatives/hypnotics stimulate:

A

GABA

241
Q

MCly used Sedatives/hypnotics are:

A

Benzodiazepines (one of the most frequent prescribed drugs in the world)

242
Q

Examples of Benzodiazepines: (6)

A

1) Xanax
2) Librium
3) Valium
4) Dalmane
5) Versed
6) Halcion

243
Q

Adverse effects of Benzodiazepines (8)

A

1) Over-sedation
2) Effects combined w/ other CNS depressants
3) Disinhibition
4) Depression
5) Cognitive impairment
6) Pregnancy adverse effects
7) Abuse
8) Tolerance/dependence/withdrawal

244
Q

Signs & Symptoms of Serotonin Syndrome:

A

“MADAMS TIPS”
- Mental status change
- Agitation
- Diarrhea
- Ataxia
- Myoclonuc
- Shivering

  • Tremor
  • Increased Reflexes
  • Pyrexia
  • Sweating
245
Q

Serotonin Syndrome is the result of excess:

A

5-HT

246
Q

Drugs that can create serotonin syndrome:

A

1) SSRI’s
2) NSSRI’s
3) Cocaine, Amphetamines, Codeine
4) Dextromethorphan

247
Q

Ephedrine & Pseudoephedrine were originally obtained from:

A

Ephedra Mahuang

248
Q

MOI of amphetamines:

A

Cause the release of catecholamines at the neuron PRESYNAPTIC terminal

249
Q

Long-term effects of Crystal meth use:

A

1) brain damage
2) weight loss
3) tooth decay “meth mouth”
4) formication (bugs crawling on skin)

250
Q

Treatment for amphetamine overdose: (3)

A

1) activated charcoal
2) DO NOT induce vomiting
3) maintain & support airway

251
Q

Match the following:

1) Spathiphyllum spp. - Poinsetta
2) Philodendron spp. - Holly
3) Toxicodendron radicals. - Peace lilly
4) Nerium oleander. - Philodendron
5) Ilex spp. - Pokeweed, Inkberry
6) Euphorbia pulcherrima. - Oleander
7) Phytolacca americana. - Poison Ivy

A

1) Spathiphyllum spp. (6) Poinsetta
2) Philodendron spp. (5) Holly
3) Toxicodendron radicals. (1) Peace lilly
4) Nerium oleander. (2) Philodendron
5) Ilex spp. (7) Pokeweed, Inkberry
6) Euphorbia pulcherrima. (4) Oleander
7) Phytolacca americana. (3) Poison Ivy

252
Q

What does Demulcent therapy consist of?

A

Ice cream, Milk & Egg whites

253
Q

General management of a plant poisoned Patient (4)

A

1) Observe Patient
2) Demulcent Therapy
3) Activated Charcoal
4) Cathartics (remove remaining material)

254
Q

What aspect of pokeweed is the most toxic?

A

Roots & leaves (fruit = mild)

255
Q

What is the toxic principle of pokeweed?

A

Resinous material & a water soluble saponin

256
Q

Clinical signs of Poke weed poisoning:

A

1) Burning sensation in the mouth
2) GI cramps
3) Vomiting, diarrhea
4) visual disturbances
5) Diaphoresis
6) Salivation

257
Q

What do you have to do to prepare pokeweed correctly?

A

Boil the leaves twice

258
Q

Treatment for pokeweed poisoning: (2)

A

1) Activated charcoal
2) Transport

259
Q

Arum family plants contain:

A

Calcium Oxalate crystals

260
Q

Members of the Arum family of plants (3)

A

1) Caladium
2) Dieffenbachia (dumbcane)
3) Philodendron

261
Q

Where in the plant are calcium oxalate crystals found in the Arum family?

A

Stalk = most severe
But are located everywhere

262
Q

Biting into an Arum family plant causes (3)

A

1) Pain & Irritation to mouth (salivation)
2) Edema
3) Choking

263
Q

Treatment for Arum Ffamily plant poisoning:

A

Supportive care & Demulcent Therapy

264
Q

Mistletoe berries contain

A

Tyramine & Phenylethylamine

265
Q

Clinical Signs of Mistletoe poisoning:

A

1) Acute Gastroenteritis
2) Cardiovascular collapse
3) respiratory difficulty
4) nausea & vomiting
5) delirium & hallucinations
6) death

266
Q

Treatment for Mistletoe poisoning:

A

Activated charcoal & transport

267
Q

Are poinsettias toxic?

A

No, but they contain a latex sap leading to irritation of the mucous membranes

268
Q

Treatment for poinsettia irritation:

A

Demulcent therapy

269
Q

Cardiotoxic plants contain:

A

Cardiac Glycosides

270
Q

Examples of Cardiotoxic plants:

A

Oleander, Azaleas & Lilly of the Valley

271
Q

MOI of Cardiotoxic plants:

A

Bind to cell membrane & inhibit the Na/K pump

272
Q

Clinical signs of Cardiotoxic Plant poisoning:

A

Heart block
Brady or Tachycardia
V-fib

273
Q

Clinical signs of Oleander poisoning:

A

1) GIT irritation
2) abdominal pain & vomiting/Diarrhea
3) Hyperkalemia
4) AV Block / cardio genie shock

274
Q

Treatment for Oleander Poisoning:

A

1) Induce Vomiting
2) Activated charcoal
3) Transport

275
Q

What portion of poison ivy plant is toxic?

A

ALL; even smoke from burning it

276
Q

What is the toxic principle found in poison ivy?

A

Oily Oleoresin called Urushiol

277
Q

Clinical signs of Poison Ivy poisoning: (4)

A

1) contact dermatitis
2) blistering
3) inflammation
4) vesicle formation

278
Q

Poison Ivy treatment: (5)

A

1) Epsom salt
2) Electronic itch stopper
3) Tecnu cleanser
4) corticosteroids
5) histamine blockers

279
Q

Plants other than Poison ivy that contain Urushiol:

A

1) Cashew nut shells
2) mango tree
3) Ginkgo tree

280
Q

Clinical signs of Capsicum Annuum “pepper pant”: (2)

A

GIT upset & Diarrhea

281
Q

Treatment for Capsicum Annuum “pepper plant” poisoning:

A

Demulcent therapy

282
Q

What are the MCly used insecticides in the world?

A

Organophosphates

283
Q

What type of Insecticides are responsible for the most poisonings?

A

Organophosphates

284
Q

MOI of Organophasphates:

A

Indirect acting Cholinomimetics (directly inhibit ACh)
ACh + ACHase -> Choline + Acetyl-ACHase
Acetyl-ACHase + H20 -> Acetic Acid + ACHase
OP + ACHase -> Phosphorylated ACHase
Phosphorylated ACHase + ACH -> No Reaction

285
Q

The MOI reaction seen in Organophosphates is __________ and takes _________ for ACh levels to return to normal.

A

Irreversible; 4 weeks

286
Q

What is the basic problem regarding ACH in Organophosphate toxicity?

A

ACHase is inhibited; therefore ACh accumulates at the POSTSYNAPTIC synapse over stimulating the Cholinergic receptors

287
Q

Muscanaric Clinical features due to over stimulation of the cholinergic receptors….

A

Over stimulation of parasympathetic & sympathetic organs that are stimulated by ACh

288
Q

Nicotinic Clinical features due to over stimulation of the cholinergic receptors….

A

Spastic paralysis of skeletal muscle in high levels

289
Q

Parasympathetic over stimulation of muscarinic receptors in OP poisoning results in: DUMBELS Analogy

A

1) Diarrhea
2) Urination
3) Miosis
4) Bronchspasm, Bronchorrhea
5) Emesis
6) Lacrimation
7) Salivation

290
Q

Over stimulation of the Sympathetic muscarinic receptors in OP poisoning can result in… (4)

A

1) Diaphoresis
2) Anxiety
3) Ataxia
4) Respiratory & Circulatory Collapse

291
Q

Over stimulation of the Sympathetic Nicotinic receptors in OP poisoning can result in… (4)

A

1) Muscle Fasciculations
2) Muscle cramps
3) Seizures
4) Respiratory difficulty

292
Q

In OP Poisoning, death is usually due to…

A

Respiratory failure

293
Q

Chronic OP ingestion can cause… (3)

A

1) Proximal muscle weakness due to motor end plate degeneration
2) Axonal Degeneration
3) Peripheral neuropathy

294
Q

How do you diagnose OP Toxicity?

A

Via RBC Cholinesterase levels
(10 mls of blood in a green top tube)

295
Q

Treatment for OP Poisoning:

A

1) Activated charcoal
2) Remove clothing & wash w/ soap. Rinse with ethyl alcohol
3) Antidotes

296
Q

What are the 2 antidotes for OP poisoning?

A

1) Atropine
2) Pralidoxine (2-PAM Chloride) can reverse phosphorylation of AChE

297
Q

What is the Most toxic OP?

A

TEPP (Tetraethyl Pyrophosphate)

298
Q

Examples of OP’s: (3)

A

1) Chlorpyifos (Dursban)
2) Diazinion
3) Malathion

299
Q

Carbamates are derived from:

A

Carbamic acid

300
Q

What are Carbamates?

A

Reversible Cholinesterase Inhibitors

301
Q

Difference between OP’s and Carbamates

A

Signs & Symptoms are similar, but Carbamates are more benign and shorter in duration.
Carbamates do not show CNS Signs

302
Q

Treatment for Carbamates toxicity:

A

1) Activated charcoal
2) remove clothing & wash w/ soap. Rinse with Ethyl Alcohol
3) use antidotes (same as OP’s)

303
Q

MOI for Organochlorines:

A

Inhibit GABA receptor and Prevent Cl- influx in the CNS

304
Q

Organochlorides mainly affect:

A

CNS & CVS

305
Q

Clinical presentation of Acute Organochloride toxicity: (6)

A

1) Nausea, vomiting
2) Seizures
3) Apprehension / confusion
4) Muscle twitching
5) Face paresthesias
6) respiratory failure

306
Q

Clinical presentation of Chronic Organochloride toxicity: (7)

A

1) Anorexia
2) Hepato & Renal toxicity
3) CNS disturbances
4) skin irritation
5) weight loss
6) Paresis
7) Neoplasia

307
Q

Treatment for Organochloride toxicity:

A

Protect airway, Activated charcoal, supportive care

308
Q

What insecticide is derived from the flowers of Chrysanthmum?

A

Pyrethrum

309
Q

Which insecticide has a very low mammalian toxicity?

A

Pyrethrum

310
Q

Pyrethrum exposure can cause (5)

A

1) Nausea, vomiting
2) Hyperexcitability
3) allergic rhinitis
4) dermatitis
5) Asthma & cough

311
Q

Treatment for Pyrethrum toxicity

A

Adam’s flea spray

312
Q

Excessive topical use of DEET has been linked with

A

Toxic encephalopathy

313
Q

Clinical features of DEET toxicity: (6)

A

1) Lethargy
2) Anxiety
3) Ataxia
4) Seizures, Coma
5) Irritant dermatitis
6) Conjunctivitis

314
Q

What can you place in your basement to prevent insects? What does it contain that works?

A

Bois’d arc fruit (Horse apples)
Contains Elemol

315
Q

What is the phone # for poison emergency?

A

1 (800) 222-1222

316
Q

General approach to poison treatment:

A
  • If victim has collapsed/not breathing call 911
  • ABC’s: airway, breathing, cardiac
  • Decontaminate the gut, clothing, skin
  • Monitor vital signs
  • Unconcious? -> Maintain Airway
317
Q

If a poison victim is convulsing… (5)

A

1) DO NOT stick fingers in mouth
2) get them to the middle of the floor
3) remove constrictive clothing
4) keep stimuli to a minimum
5) Call 911

318
Q

Child 1 swallow = ?
Adult 1 swallow = ?

A

Child -> 1 teaspoon
Adult -> 1 Tablespoon

319
Q

3 ways to prevent absorption of a poison:

A

1) Gastric evacuation
2) Administer Absorbent
3) Catharsis

320
Q

Syrup of Ipecac is a…

A

Emetic

321
Q

Emetine & Cephaline are…

A

Syrup of Ipesac’s

322
Q

Emetine works where in th body?

A

Systemically & locally. Has a cumulative toxic effect on the heart

323
Q

What is Cephaline?

A

Direct GI irritant that is twice as potent as Emetine

324
Q

Who should you give Syrup of Ipecac to?

A
  • Only alert pt’s w/ gag reflex
  • over 6 months old
325
Q

Never repeat a dose of Ipecac more than _____________ after first administration

A

20 minutes

326
Q

When should you NOT give Ipecac? (5)

A

1) At home
2) Pt. Is less than 1 year old
3) If oven cleaners, dishwasher detergent or other strong acids/bases (corrosives) have been taken
4) Kerosene, gasoline, paint thinner, furniture polish has been taken
5) Pt. Is Lethargic or Convulsing

327
Q

What is “gastric lavage”?

A

Pumping the stomach

328
Q

What does Ionized dieresis do?

A

Facilitates excretion of poisons that are eliminated through the kidneys

329
Q

Once an absorbent binds to the poison is is excreted through…

A

The feces

330
Q

Substances that are not well absorbed by Activated charcoal: (6)

A

1) Lithium
2) Strong acids/bases
3) Metals (iron, lead, arsenic, iodine)
4) Flourine & boric acid
5) Alcohols & Acetone
6) Hydrocarbons (petroleum distillates & pine oil)

331
Q

What is the ratio for Activated charcoal to toxin?

A

10x Charcoal for the amount ingested

332
Q

Contraindications for Activated Charcoal: (4)

A

1) Intestine obstruction
2) Injested strong acid or base
3) Constipated
4) If antidote was used (it will get absorbed as well)

333
Q

What are cathartics?

A

Drugs that promote evacuation of the bowel
(Purgatives, laxatives)

334
Q

4 Commonly used cathartics:

A

1) Sorbitol
2) Mannitol
3) Mg Sulfate
4) Mg Citrate

335
Q

Orbital should not be used in

A

Children under 1 year old because it can lead to excess fluid loss

336
Q

MOI of Cathartics:

A

Osmotic agents that stimulate GI motility

337
Q

Contraindications for using Cathartics: (3)

A

1) Absent bowel sounds
2) CVD or Renal disease
3) Electrolyte Imbalance

Pharm Tox (3 decks)

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